Nutrition and cognition across the lifetime: an overview on epigenetic mechanisms

Arianna Polverino; Pierpaolo Sorrentino; Matteo Pesoli; Laura Mandolesi; Arianna Polverino; Pierpaolo Sorrentino; Matteo Pesoli; Laura Mandolesi

doi:10.3934/Neuroscience.2021024

AIMS Neuroscience

2021, Volume 8, Issue 4: 448-476. doi: 10.3934/Neuroscience.2021024

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Review

Nutrition and cognition across the lifetime: an overview on epigenetic mechanisms

1.
Institute of Diagnosis and Treatment Hermitage Capodimonte, Naples, Italy
2.
Department of Motor and Wellness Sciences, University of Naples “Parthenope”, Naples, Italy
3.
Institut de Neurosciences des Systèmes, Aix-Marseille University, Marseille, France
4.
Institute of Applied Sciences and Intelligent Systems, National Research Council, Pozzuoli, Italy
5.
Department of Humanities Studies, University of Naples Federico II, Naples, Italy

Received: 22 April 2021 Accepted: 12 July 2021 Published: 15 July 2021

The functioning of our brain depends on both genes and their interactions with environmental factors. The close link between genetics and environmental factors produces structural and functional cerebral changes early on in life. Understanding the weight of environmental factors in modulating neuroplasticity phenomena and cognitive functioning is relevant for potential interventions. Among these, nutrition plays a key role. In fact, the link between gut and brain (the gut-brain axis) is very close and begins in utero, since the Central Nervous System (CNS) and the Enteric Nervous System (ENS) originate from the same germ layer during the embryogenesis. Here, we investigate the epigenetic mechanisms induced by some nutrients on the cognitive functioning, which affect the cellular and molecular processes governing our cognitive functions. Furthermore, epigenetic phenomena can be positively affected by specific healthy nutrients from diet, with the possibility of preventing or modulating cognitive impairments. Specifically, we described the effects of several nutrients on diet-dependent epigenetic processes, in particular DNA methylation and histones post-translational modifications, and their potential role as therapeutic target, to describe how some forms of cognitive decline could be prevented or modulated from the early stages of life.
- nutrition,
- cognitive functioning,
- environmental factors,
- epigenetics,
- neuroplasticity
Citation: Arianna Polverino, Pierpaolo Sorrentino, Matteo Pesoli, Laura Mandolesi. Nutrition and cognition across the lifetime: an overview on epigenetic mechanisms[J]. AIMS Neuroscience, 2021, 8(4): 448-476. doi: 10.3934/Neuroscience.2021024

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Abstract

The functioning of our brain depends on both genes and their interactions with environmental factors. The close link between genetics and environmental factors produces structural and functional cerebral changes early on in life. Understanding the weight of environmental factors in modulating neuroplasticity phenomena and cognitive functioning is relevant for potential interventions. Among these, nutrition plays a key role. In fact, the link between gut and brain (the gut-brain axis) is very close and begins in utero, since the Central Nervous System (CNS) and the Enteric Nervous System (ENS) originate from the same germ layer during the embryogenesis. Here, we investigate the epigenetic mechanisms induced by some nutrients on the cognitive functioning, which affect the cellular and molecular processes governing our cognitive functions. Furthermore, epigenetic phenomena can be positively affected by specific healthy nutrients from diet, with the possibility of preventing or modulating cognitive impairments. Specifically, we described the effects of several nutrients on diet-dependent epigenetic processes, in particular DNA methylation and histones post-translational modifications, and their potential role as therapeutic target, to describe how some forms of cognitive decline could be prevented or modulated from the early stages of life.

Abbreviations

Alzheimer's disease

ALS

Amyotrophic Lateral Sclerosis

BDNF

Brain-Derived Neurotrophic Factor

BMI

body mass index

CBP

CREB-binding protein

CNS

Central Nervous System

DHA

docosahexanoic acid

DNMT

DNA methyl-transferase

DOHaD

Developmental Origin of Health and Disease

EGCG

epigallocatechin gallate

ENS

Enteric Nervous System

EPA

eicosapentaenoic acid

FAS

fetal alcoholic syndrome

FASD

fetal alcohol spectrum disorders

FTD

Frontotemporal Dementia

HATs

histone acetyl-transferases

HCY

homocysteine

HDACs

histone deacetylases

HMTs

histone methyl-transferases

IGF-2

Insulin-like growth factor-2

LCPUFAs

long chain polyunsaturated fatty acids

LOAD

late onset Alzheimer's disease

MCI

mild cognitive impairment

MeCP2

methyl-CpG-binding protein

Parkinson's disease

POHaD

Paternal Origin of Health and Disease

RAR-α

retinoic acid receptor-α

SAH

S-adenosyl-homocysteine

SAM

S-adenosyl-methionine

SCFAs

short-chain fatty acids

VAD

vitamin A deficiency

VDR

vitamin D receptor.

Acknowledgments

This study was supported by funding from the Project “Bando Ricerca Competitiva 2017”, University of Naples Parthenope (D.R.289/2017) to L.M. and from the Department of Humanities, University of Naples Federico II (Fondi ricerca dipartimentale 2020 and 2021) to L.M.

Conflict of interest

All authors declare no conflicts of interest.

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